Tuesday, 6 October 2015


Interview with Prof. Ying Zhang at the NorVect Conference 2015

Published on Sep 29, 2015
Prof Ying Zhang from John Hopkins Bloomberg School of Public Health explains why Lyme disease is so difficult to treat. Having worked with Tuberculosis (TB) for many years, he sees the similarities and differences between these to bacteria. With Tuberculosis it is known that you have to treat with certain drug combinations that kill the growing form and the non-growing form (persisters) and if you treat shorter than 6 months, the patient will get a relapse.

The bacterium that causes Lyme disease is much more advanced than the TB bacterium, and the main reason is that it also takes a persisting form. These persister forms of the Borrelia bacteria cannot be cultured.

The two views – ILADS and IDSA are two different ways of seeing the same disease. Prof. Zhang thinks they are both right. When it comes to acute Lyme disease, IDSA is right. Then you only need shorter courses of treatment. When the disease turns chronic, longer courses of treatment with the right drug combinations are needed (ILADS view).

The full presentation from Dr Zhang is available on the Norvect website from their 2015 conference http://norvect.no/about-norvect/    

From Norvect website -
Talk: Borrelia Persister Drugs: Implications for Improved Treatment

Dr Zhang also presented at a recent conference in Cambridge UK, organised by Lyme Disease Action presentations will be available on their website shortly

It was a wonderful opportunity to hear Dr Zhang present and also to have opportunity to discuss his work.

Dr Zhang told me that he studied at Birmingham University and later in London (I think he said UCL) - somewhat ironic for me in view of our Health Authorities head in the sands denial of chronic Lyme Disease, that this leading researcher in this field of why and how Borrelia persists, was trained at two of our Universities.

I have posted previously about Dr Zhang's work 

Wednesday, 23 September 2015


ILADS treatment guidelines are now listed on the National Guidelines Clearinghouse Website.

(Sept 21, 2015) — The Centers for Disease Control and Prevention (CDC) estimates that more than 300,000 new cases of Lyme disease occur annually in the US. ILADS guidelines, Evidence Assessments and Guideline Recommendations in Lyme disease: The Clinical Management of Known Tick Bites, Erythema Migrans Rashes and Persistent Disease” bring the latest scientific evidence to bear on the management of the illness. ILADS is proud to announce their guidelines are now available on the National Guidelines Clearinghouse (NGC) website.

The National Guidelines Clearinghouse (NGC) is an initiative of the Agency for Healthcare Research and Quality (AHRQ), under the umbrella of the U.S. Department of Health and Human Services. The NGC recently adopted the Institute of Medicine (IOM) standards for developing trustworthy guidelines, which define the highest level of excellence that a guideline can achieve. Guidelines posted on the NGC website must now satisfy these standards. Thus, the inclusion of ILADS’s peer reviewed guidelines on the NGC website demonstrates that they meet the level of excellence called for by the IOM.  

ILADS is the first organization to issue guidelines on Lyme disease that were developed in accordance with the IOM standards. The document provides a detailed review of the pertinent medical literature and contains the first set recommendations for Lyme disease based on the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) process. This rigorous review format is also used by many other well-respected medical organizations including the World Health Organization (WHO), the American College of Physicians, and the National Institute for Health and Clinical Excellence (NICE) in the UK. ILADS guidelines are the only Lyme disease guidelines that included a patient from the Lyme community as an author or as a member of the guidelines development panel.

ILADS’ GRADE-based analyses found the evidence was of very low quality and regimens based on randomized controlled trials often failed. “For this reason, we moved away from designating a fixed duration for antibiotic therapy and instead encourage clinicians to tailor therapy based on the patient’s response,” noted Cameron, author and president of ILADS.

“We not only recommend that clinicians perform a deliberate and individualized assessment of the potential risks and benefits of various treatment options before making their initial selection, we also recommend careful follow-up because this allows them to adjust therapy as circumstances evolve.  This patient-centered approach should reduce the risk of chronic illness due to inadequate antibiotic therapy.” said Elizabeth Maloney, MD, a guidelines coauthor and provider of continuing medical education courses on tick-borne illnesses.

The guidelines include share medical decision making and take patient values into consideration. Lorraine Johnson, JD, MBA, a coauthor and Chief Executive Officer of LymeDisease.org, said “A lot of the treatment decisions in Lyme disease depend on trade-offs. How sick is the patient, how invasive is the treatment, what is valued by the patient? Patients need to understand the risks and benefits of treatment options to make informed medical choices. These guidelines provide that information.”

ILADS is a nonprofit, international, multidisciplinary medical society dedicated the appropriate diagnosis and treatment of Lyme and associated diseases. For more information, visit www.ILADS.org.
The above was from an E mail from ILADS 21st September 2015


The best possible news for Lyme Disease patients around the World. This means that the outdated IDSA guidelines which are currently in the process of being updated are no longer the sole voice on treatment options for patients.
Although many doctors and patients have followed earlier guidelines from ILADS they were strongly criticized because they were not fully referenced and not peer reviewed. This is no longer the case with these new guidelines and so must now be considered when looking at helping patients. 
The UK guidance is over due to be revised, it was promised by PHE a couple of years ago but recently we have been informed that it will be a NICE process, thus putting completion off further to 2018. 

In 2013 the James Lind Alliance research found many uncertainties in guidance that is held on PHE website. The Dept of Health and PHE were involved in that James Lind Alliance process so are fully aware of the limitations of evidence to support the current guidance for the NHS. Failing to inform doctors of the limitations would appear to be negligent and has resulted in many patients being refused treatment based on PHE guidance.

As NICE develops new Guidance they must now also consider the ILADS Guidelines 

Friday, 18 September 2015


'We shouldn't accept chronic mental illnesses as something that is there we can prevent it, treat it and understand it better.' Dr Robert Bransfield 

Published on Nov 5, 2014
Dr. Robert Bransfield provided this very informative talk on the psychiatric and neuropsychiatric manifestations of tick-borne diseases at the "Symposium on Tick-borne Diseases" held on May 17, 2014 at the Hyatt in Cambridge, Maryland. The conference was hosted by the Lyme Disease Association of the Eastern Shore of Maryland, a 501(c)(3) non-profit organization providing educational resources on tick-borne diseases. We are 100% dependent upon donations to continue providing educational resources such as this video. Please consider supporting our efforts. LDAESM, P.O. Box 5360, Salisbury, MD 21802 Thank you!

Interesting to hear that Lyme induced Autism often tests positive on Bands 31 and 34 - these two bands were removed from the two tier testing, due to conflicts with vaccine production - but as Dr Bransfield says in the presentation this raises great concerns in the use of the Outer surface proteins ( linked to bands 31 and 34) in vaccine production and it's possible bearing on the Autism epidemic being escalated even further. 

'The two tier testing used for Lyme Disease is useless it's dangerous.'

'Immune mediated effects of Lyme/Tick borne diseases contributes to cognitive impairments, dementia, depression, anxiety, Autism, violence and other psychiatric illnesses.'

'We have insights into preventing a lot of chronic diseases, a lot of pain, a lot of suffering violence death - and particularly the Autism.'

Good to listen to Dr Bransfield once again - I have heard him present in the UK on two occasions. 

Previous posts on Dr Bransfield  click here 

Dr Bransfield's website http://www.mentalhealthandillness.com/

Wednesday, 19 August 2015


Persister mechanisms in Borrelia burgdorferi: implications for improved intervention

Jie Feng, Wanliang Shi, Shuo Zhang and Ying Zhang
Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA

Citation: Emerging Microbes & Infections (2015) 4, e51; doi:10.1038/emi.2015.51
Published online 19 August 2015

Received 11 July 2015; Revised 1 August 2015; Accepted 5 August 2015

Lyme disease caused by Borrelia burgdorferi is the most common vector borne disease in the United States and Europe.1,2 The current treatment for Lyme disease is a 2-4 week antibiotic monotherapy with doxycycline, amoxicillin or cefuroxime.3 While this treatment is effective for the majority of Lyme disease patients, about 10%-20% of patients still have persisting symptoms such as fatigue, muscular pain, and neurological impairment even six months after the treatment,1 a collection of symptoms called Post Treatment Lyme Disease Syndrome (PTLDS).4 While the cause of PTLDS remains unclear and controversial, several hypotheses have been proposed to explain PTLDS, including host response to continued presence of bacterial debris,5 autoimmunity,6 co-infections,7 and presence of bacterial persisters not killed by the current Lyme antibiotics.7Consistent with the persisting organisms not killed by current antibiotics, experiments in various animal models such as mice, dogs and monkeys have shownB. burgdorferi could still be detected after treatment with different Lyme antibiotics though viable organisms could not be cultured.8,9,10 In vitro studies also demonstrated that B. burgdorferi could develop antibiotic tolerant persisters.11 Although persister mechanisms have been reported in the model organism E. coli,12 the mechanisms of B. burgdorferi persisters remain unknown.

Our findings not only shed new light on the mechanisms of B. burgdorferipersisters but also have practical applications. For example, the upregulated genes identified in B. burgdorferi persisters may not only serve as targets for developing new drugs for more effective treatment but also antigens for developing diagnostic tests for persistent Lyme disease, and finally for developing therapeutic vaccines for improved treatment. Future studies are needed to address these possibilities for more effective control of Lyme disease.

Dr Horowitz summed it up:-

Major universities are finally taking an interest in persister bacteria and their role in contributing to chronic symptoms in patients with Lyme disease. Dr Ying Zhang and researchers from Johns Hopkins University just published on Borrelia persisters in Emerging Microbes and Infections where they identified the gene expression profile for Bb persisters that survived antibiotic treatment with doxycycline and amoxicillin. They found differences in transporter genes, bacterial envelope protein coding genes, DNA repair related genes, bacterial chemotaxis genes, bacterial secretion genes, and genes encoding proteases. Comparison of the pathways of the doxycycline persisters and amoxicillin persisters revealed that they share several common features where some genes were up regulated and some down regulated. "These gene expression changes may play important roles in facilitating survival of B. burgdorferi persisters under antibiotic stress...and the upregulated genes identified in B. burgdorferi persisters may not only serve as targets for developing new drugs for more effective treatment but also antigens for developing diagnostic tests for persistent Lyme disease, and finally for developing therapeutic vaccines for improved treatment". The MSIDS map identifies up to 16 different reasons why patients may stay ill after classical treatment for Lyme disease. Persistent infection with borrelia species and co-infections certainly plays a large role in chronic illness, but we must also treat associated inflammation, autoimmune reactions, detoxify internal and external biotoxins, repair the damage caused by free radicals and oxidative stress which damage mitochondria, nerves, brain cells and internal organs, while balancing cytokines, hormones, and the microbiome. Once all of the associated factors on the 16 point MSIDS map have been adequately addressed, the vast majority of my patients improve. A large thanks goes out to the Global Lyme Alliance for their support of this research, and to Dr Zhang and his colleagues at Johns Hopkins for continuing to search for answers for this debilitating illness.

Sunday, 26 July 2015


Alzheimer's Disease
Studied with Autopsy demonstrates  that Infection by Borrelia Spirochetes
is regularly present in Autopsy Alzheimer's Disease brains. The Chronic Borrelia Brain Infection is a Cause of Alzheimer's Disease.

The Model  for  Dementia CAUSED by Chronic  brain Infections by Spirochetes is the conclusive Model of Dr. Hideyo Noguchi  who proved that Treponema Pallidum  late chronic Brain Infection is  THE CAUSE  of General Paresis 
[ Syphilis dementia]

21st century tools investigate infection by detection of microbe's DNA at the site of the Disease in human tissue.

DNA of Borrelia is Present in the following areas of the Alzheimer's Brain:
1.  All of the Alzheimer's Plaques
2.  Perfect Spirochetes (Borrelia) are seen under the fluorescent microscope
       in solid brain tissues, in Blood vessels of the Brain, and in the   Alzheimer's Plaques.
3.  All of the Granular bodies which are present in dying nerve cells in the     Alzheimer's Brain
        (Granulo-vacuolar Degeneration: {GVB Lesions]
Autopsy Brain, when placed in Laboratory Cultures produce pure Cultures of Borrelia spirochetes.

My present Research uses DNA Probes , specific for borrelia , to bind to  sites in diseased brain tissues, specifically Alzheimer's Disease Autopsy Brain tissues.

FISH methods (Fluorescence In Situ DNA Hybridization)-  in my research -  utilizes the BEST DNA PROBES available today, specifically Molecular Beacons.  The Molecular Beacons absolutely bind to Target Borrelia DNA ...
but only will bind to a DNA .. if There is a 100% match-
between TheMicrobe Borrelia DNA in diseased tissues - and the DNA structure in My  Molecular Beacon DNA Probes...
            If even a single Base (nucleotide "A"or"T" ,or"G", or "C") Mismatch exists, .. the 100% rule for Molecular Beacon Binding is Violated,.
and no signal will be released by the DNA probe.  A positive signal indicates that the 100% match rule for Molecular Beacon DNA Probe binding has been satisfied.  A Positive FISH Hybridization in Alzheimer's Brain,  is Bulletproof evidence of Borrelia infection - Visualized by the Fluorescent Microscope.
FISH Borrelia Probes Visualize ENTIRE Borrelia spirochetes - at the EXACT sites of Alzheimer's tissue injuries..

In a Series of  cases from the Harvard Brain Bank ,

         [from Alzheimer's Disease Brains]..
my Molecular Beacon DNA Probes bound to Borrelia DNA in ALL CASES STUDIED. (5/5)

The astonishing observation in my DNA probe studies on the Harvard Brain Bank Alzheimer's Disease Cases is the Discovery of not just One Borrelia,  But, Two strains of borrelia in five of five Alzheimer' s brains...
Two different   species of Borrelia spirochetes
(Burgdorferi and Miyamotoi)  were simultaneously present in the Alzheimer's Brain tissues, from Harvard.

The Discovery of Burgdorferi  in Alzheimer's Brain was FIRST published by me in the Journal of the American Medical Association in 1986.  
I demonstrated Borrelia spirochetes from 4 cases obtained from Dr. George Glenner's Brain Bank at the UCSD SanDiego.
I succeeded in a total of 6 Alzheimer's Cases in the culture in the laboratory of Living Borrelia spirochetes from DEAD (Autopsy Brain) tissue., between 1986 to 1988. 
Subsequently, in year 1993,  Cultures for borrelia from Autopsy Alzheimer's disease  was again verified by Dr. Judith Miklossy, in Switzerland.

In year 2015, my research continues, with DNA probes specific for Borrelia DNa in Alzheimer's tissue. I request your support to extend my DNA Probe studies
to connect Chronic Deep Brain Infection with Borrelia Burgdorferi and Borrelia Miyamotoi in Alzheimer's patients. I want to extend my research to study the
Spinal fluid from living Donor patients with Dementia to detect Borrelia DNA in the spinal Fluid.

Early Detection of Borrelia Brain Infection offers the opportunity for the patient to be treated in the hope that ERADICATION of Brain and Spinal Fluid Infection, can Prevent the Development of Dementia.

I thank you for your support.  All of my research has always been FREE for All , and will remain Free for All.
None of my discoveries have been or ever will be patented .  No patient / volunteer will ever be charged for my research on their Behalf.

Respectfully submitted,

Alan B. MacDonald,MD
Fellow, College of American  Pathologists

8427 Benelli Court
Naples. Florida, 34114, USA

Note: Additional Video Lectures on my Alzheimer's Research  are FREEly available on You Tube and Vimeo.

My Website:

I have posted Images /Galleries of Borrelia spirochetes
under Fluorescent Microscopy  using my FISH method
and my Borrelia Specific DNA Probes:



Taken and shared from Dr MacDonald's Fund Raiser - raising funds for further research into the links between various Borrelia species and Alzheimer's.

Please give generously and share this fundraiser among your friends (also at this link Dr MacDonald has updated details and presentations on his important work)

Link to Poster presentation of Dr MacDonald's research http://f1000research.com/posters/4-631

Friday, 24 July 2015


Penetration of doxycycline into cerebrospinal fluid in patients treated for suspected Lyme neuroborreliosis.

  1. L Hagberg

      Twelve patients were treated orally with 100 mg of doxycycline twice a day (b.i.d.) and 10 patients were treated with 200 mg b.i.d. for suspected tick-borne neuroborreliosis (Lyme borreliosis). At 5 to 8 days after the start of therapy, the mean concentrations in serum were 4.7 micrograms/ml for the doxycycline dose of 100 mg b.i.d. and 7.5 micrograms/ml for 200 mg b.i.d., 2 to 3 h after the last drug administration. The corresponding levels for cerebrospinal fluid were 0.6 and 1.1 micrograms/ml. Since a doxycycline concentration in cerebrospinal fluid above the estimated MIC for Borrelia burgdorferi (0.6 to 0.7 microgram/ml) is wanted in patients treated for severe neuroborreliosis, the higher dose is preferable.
    2. Minocycline versus Doxycycline in the Treatment of Lyme Neuroborreliosis

    3. 'It is not commonly appreciated that ill patients treated with doxycycline (e.g., patients with legionnaires' disease) should be given a loading regimen of 200 mg iv q12h for the first 72 h, because of doxycycline's lipid solubility characteristics and long half-life. Since 5 serum half-lives are usually required to achieve steady-state serum concentrations, and early therapeutic effect, a loding regimen rather than a loading dose permits rapid saturation of the serum. If doxycycline is administered in the usual dosage of 100 mg q12h, then it takes 4–5 days to achieve steady-state kinetics and an observable therapeutic response. In Lyme neuroborreliosis, rapid saturation of the CNS compartment is key to the efficacy of short-course regimens (≤14 days). Doxy-cycline is usually given in dosages of 100 mg q12h, which means that the first week of treatment is virtually lost in achieving steady-state equilibrium, and equilibrium results require 3 weeks [710]. Dotevall and Hagberg correctly used 400 mg of doxycycline daily and decreased treatment time to ∼10.8 days.'

    4. Although the above articles were published some years ago I have posted them because they support the need for a higher dose of Doxycycline in the treatment of early Lyme Neuroborreliosis. A concept foreign to most of our doctors. Lyme Neuroborreliosis is when the bacteria affect the nervous system and the symptoms are many and varied the best resource for details about Lyme Neuroborreliosis is found in the leaflet Lyme Disease Action have on the subject. It is easy for patients and doctors to say it is suspected Lyme Disease and fail to realise the significance of nervous system symptoms indicating Lyme Neuroborreliosis.

Sunday, 5 July 2015


Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection


Lyme Disease caused by infection with Borrelia burgdorferi is an emerging infectious disease and already by far the most common vector-borne disease in the U.S. Similar to many other infections, infection with Bburgdorferi results in strong antibody response induction, which can be used clinically as a diagnostic measure of prior exposure. However, clinical studies have shown a sometimes-precipitous decline of such antibodies shortly following antibiotic treatment, revealing a potential deficit in the host’s ability to induce and/or maintain long-term protective antibodies. This is further supported by reports of frequent repeat infections with B.burgdorferi in endemic areas. The mechanisms underlying such a lack of long-term humoral immunity, however, remain unknown. We show here that Bburgdorferi infected mice show a similar rapid disappearance of Borrelia-specific antibodies after infection and subsequent antibiotic treatment. This failure was associated with development of only short-lived germinal centers, micro-anatomical locations from which long-lived immunity originates. These showed structural abnormalities and failed to induce memory B cells and long-lived plasma cells for months after the infection, rendering the mice susceptible to reinfection with the same strain ofBburgdorferi. The inability to induce long-lived immune responses was not due to the particular nature of the immunogenic antigens of Bburgdorferi, as antibodies to both T-dependent and T-independent Borrelia antigens lacked longevity and B cell memory induction. Furthermore, influenza immunization administered at the time of Borrelia infection also failed to induce robust antibody responses, dramatically reducing the protective antiviral capacity of the humoral response. Collectively, these studies show that Bburgdorferi-infection results in targeted and temporary immunosuppression of the host and bring new insight into the mechanisms underlying the failure to develop long-term immunity to this emerging disease threat.

Author Summary

Infections with the Lyme Disease agent, Borrelia burgdorferi, often fail to generate long-term protective immunity. We show here that this is because the immune system of the Borrelia-infected host generates only short-lived, structurally abnormal and non-functional germinal centers. These germinal centers fail to induce memory B cells and long-lived antibody-producing plasma cells, leaving the host susceptible to reinfection with Bb. This inability to induce long-term immunity was not due to the nature of Borrelia antigens, as even T-dependent antigens of Borrelia were unable to induce such responses. Moreover, influenza vaccine antigens, when applied during Borrelia-infection, failed to induce strong antibody responses and immune-protection from influenza challenge. This data illustrate the potent, if temporal, immune suppression induced by Borrelia-infection. Collectively, the data reveal a new mechanism by which Bburgdorferi subverts the adaptive immune response.